Limits...
Isocryptotanshinone Induced Apoptosis and Activated MAPK Signaling in Human Breast Cancer MCF-7 Cells.

Zhang X, Luo W, Zhao W, Lu J, Chen X - J Breast Cancer (2015)

Bottom Line: Apoptosis was determined by Hoechst 33342 staining, DNA fragmentation assays, and Western blotting for apoptotic proteins.ICTS significantly inhibited proliferation of MCF-7 and MDA-MB-231 human breast cancer cells, HepG2 human liver cancer cells, and A549 human lung cancer cells in vitro.Hoechst 33342 staining and Western blot analysis for apoptotic proteins suggested that ICTS induced apoptosis in MCF-7 cells.

View Article: PubMed Central - PubMed

Affiliation: State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao, China.

ABSTRACT

Purpose: Isocryptotanshinone (ICTS) is a natural bioactive product that is isolated from the roots of the widely used medical herb Salvia miltiorrhiza. However, few reports exist on the mechanisms underlying the therapeutic effects of ICTS. Here, we report that ICTS has anticancer activity and describe the mechanism underlying this effect.

Methods: The antiproliferative effect of ICTS was determined using 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) and clonogenic assays. The effect of ICTS on the cell cycle was measured using flow cytometry. Apoptosis was determined by Hoechst 33342 staining, DNA fragmentation assays, and Western blotting for apoptotic proteins. Finally, the effect of ICTS on mitogen-activated protein kinases (MAPKs) was determined by Western blotting.

Results: ICTS significantly inhibited proliferation of MCF-7 and MDA-MB-231 human breast cancer cells, HepG2 human liver cancer cells, and A549 human lung cancer cells in vitro. Among the tested cell lines, MCF-7 cells showed the highest sensitivity to ICTS. ICTS significantly inhibited colony formation by MCF-7 cells. Furthermore, exposure of MCF-7 cells to ICTS induced cell cycle arrest at the G1 phase and decreased mitochondrial membrane potential. Hoechst 33342 staining and Western blot analysis for apoptotic proteins suggested that ICTS induced apoptosis in MCF-7 cells. In addition, ICTS activated MAPK signaling in MCF-7 cells by inducing time- and concentration-dependent phosphorylation of JNK, ERK, and p38 MAPK.

Conclusion: Our results suggest that ICTS inhibited MCF-7 cell proliferation by inducing apoptosis and activating MAPK signaling pathways.

No MeSH data available.


Related in: MedlinePlus

Effect of isocryptotanshinone (ICTS) on cell cycle distribution of MCF-7 cells. (A) Cells were treated with ICTS (0-10 µM) for 24 hours, and cell cycle distribution was analyzed using flow cytometer. (B) The percentages of each G1, S, and G2/M phase for different treatment. *p<0.05 compared with control group.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4490259&req=5

Figure 2: Effect of isocryptotanshinone (ICTS) on cell cycle distribution of MCF-7 cells. (A) Cells were treated with ICTS (0-10 µM) for 24 hours, and cell cycle distribution was analyzed using flow cytometer. (B) The percentages of each G1, S, and G2/M phase for different treatment. *p<0.05 compared with control group.

Mentions: The cell cycle distribution was determined by analysis of DNA content using PI staining. Figure 2A shows the cell cycle distribution of MCF-7 cells treated with ICTS (0-10 µM). The percentages of cells in the G1, S, and G2/M phases following treatment with different concentrations of ICTS were calculated (Figure 2B). G1 phase cell cycle arrest was observed in ICTS-treated cells. The group treated with 10 µM ICTS showed a significant increase in the proportion of G1 phase cells in comparison with the control group (p<0.05) (Figure 2B).


Isocryptotanshinone Induced Apoptosis and Activated MAPK Signaling in Human Breast Cancer MCF-7 Cells.

Zhang X, Luo W, Zhao W, Lu J, Chen X - J Breast Cancer (2015)

Effect of isocryptotanshinone (ICTS) on cell cycle distribution of MCF-7 cells. (A) Cells were treated with ICTS (0-10 µM) for 24 hours, and cell cycle distribution was analyzed using flow cytometer. (B) The percentages of each G1, S, and G2/M phase for different treatment. *p<0.05 compared with control group.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4490259&req=5

Figure 2: Effect of isocryptotanshinone (ICTS) on cell cycle distribution of MCF-7 cells. (A) Cells were treated with ICTS (0-10 µM) for 24 hours, and cell cycle distribution was analyzed using flow cytometer. (B) The percentages of each G1, S, and G2/M phase for different treatment. *p<0.05 compared with control group.
Mentions: The cell cycle distribution was determined by analysis of DNA content using PI staining. Figure 2A shows the cell cycle distribution of MCF-7 cells treated with ICTS (0-10 µM). The percentages of cells in the G1, S, and G2/M phases following treatment with different concentrations of ICTS were calculated (Figure 2B). G1 phase cell cycle arrest was observed in ICTS-treated cells. The group treated with 10 µM ICTS showed a significant increase in the proportion of G1 phase cells in comparison with the control group (p<0.05) (Figure 2B).

Bottom Line: Apoptosis was determined by Hoechst 33342 staining, DNA fragmentation assays, and Western blotting for apoptotic proteins.ICTS significantly inhibited proliferation of MCF-7 and MDA-MB-231 human breast cancer cells, HepG2 human liver cancer cells, and A549 human lung cancer cells in vitro.Hoechst 33342 staining and Western blot analysis for apoptotic proteins suggested that ICTS induced apoptosis in MCF-7 cells.

View Article: PubMed Central - PubMed

Affiliation: State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao, China.

ABSTRACT

Purpose: Isocryptotanshinone (ICTS) is a natural bioactive product that is isolated from the roots of the widely used medical herb Salvia miltiorrhiza. However, few reports exist on the mechanisms underlying the therapeutic effects of ICTS. Here, we report that ICTS has anticancer activity and describe the mechanism underlying this effect.

Methods: The antiproliferative effect of ICTS was determined using 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) and clonogenic assays. The effect of ICTS on the cell cycle was measured using flow cytometry. Apoptosis was determined by Hoechst 33342 staining, DNA fragmentation assays, and Western blotting for apoptotic proteins. Finally, the effect of ICTS on mitogen-activated protein kinases (MAPKs) was determined by Western blotting.

Results: ICTS significantly inhibited proliferation of MCF-7 and MDA-MB-231 human breast cancer cells, HepG2 human liver cancer cells, and A549 human lung cancer cells in vitro. Among the tested cell lines, MCF-7 cells showed the highest sensitivity to ICTS. ICTS significantly inhibited colony formation by MCF-7 cells. Furthermore, exposure of MCF-7 cells to ICTS induced cell cycle arrest at the G1 phase and decreased mitochondrial membrane potential. Hoechst 33342 staining and Western blot analysis for apoptotic proteins suggested that ICTS induced apoptosis in MCF-7 cells. In addition, ICTS activated MAPK signaling in MCF-7 cells by inducing time- and concentration-dependent phosphorylation of JNK, ERK, and p38 MAPK.

Conclusion: Our results suggest that ICTS inhibited MCF-7 cell proliferation by inducing apoptosis and activating MAPK signaling pathways.

No MeSH data available.


Related in: MedlinePlus